BAIT

EAF1

VID21, YDR359C
Component of the NuA4 histone acetyltransferase complex; acts as a platform for assembly of NuA4 subunits into the native complex; required for initiation of pre-meiotic DNA replication, likely due to its requirement for expression of IME1
GO Process (3)
GO Function (0)
GO Component (2)
Saccharomyces cerevisiae (S288c)
PREY

BUB2

PAC7, L000000197, YMR055C
Mitotic exit network regulator; forms GTPase-activating Bfa1p-Bub2p complex that binds Tem1p and spindle pole bodies, blocks cell cycle progression before anaphase in response to spindle and kinetochore damage
GO Process (2)
GO Function (1)
GO Component (1)

Gene Ontology Molecular Function

Gene Ontology Cellular Component

Saccharomyces cerevisiae (S288c)

Synthetic Lethality

A genetic interaction is inferred when mutations or deletions in separate genes, each of which alone causes a minimal phenotype, result in lethality when combined in the same cell under a given condition.

Publication

Regulation of chromosome stability by the histone H2A variant Htz1, the Swr1 chromatin remodeling complex, and the histone acetyltransferase NuA4.

Krogan NJ, Baetz K, Keogh MC, Datta N, Sawa C, Kwok TC, Thompson NJ, Davey MG, Pootoolal J, Hughes TR, Emili A, Buratowski S, Hieter P, Greenblatt JF

NuA4, the only essential histone acetyltransferase complex in Saccharomyces cerevisiae, acetylates the N-terminal tails of histones H4 and H2A. Affinity purification of NuA4 revealed the presence of three previously undescribed subunits, Vid21/Eaf1/Ydr359c, Swc4/Eaf2/Ygr002c, and Eaf7/Ynl136w. Experimental analyses revealed at least two functionally distinct sets of polypeptides in NuA4: (i) Vid21 and Yng2, and (ii) Eaf5 and Eaf7. Vid21 and Yng2 ... [more]

Proc. Natl. Acad. Sci. U.S.A. Sep. 14, 2004; 101(37);13513-8 [Pubmed: 15353583]

Throughput

  • High Throughput

Ontology Terms

  • inviable (APO:0000112)

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
EAF1 BUB2
Positive Genetic
Positive Genetic

Mutations/deletions in separate genes, each of which alone causes a minimal phenotype, but when combined in the same cell results in a less severe fitness defect than expected under a given condition. This term is reserved for high or low throughput studies with scores.

High-BioGRID
3530775

Curated By

  • BioGRID